PHLEBOTOMY REVERSES THE HEMODYNAMIC CONSEQUENCES OF THORACIC AORTIC CROSS-CLAMPING - RELATIONSHIPS BETWEEN CENTRAL VENOUS-PRESSURE AND CEREBROSPINAL-FLUID PRESSURE

In dogs (n = 11) anesthetized with sodium pentobarbital (to an isoelectric EEG), the authors investigated the influence of thoracic aortic cross-clamping (AXC) on systemic hemodynamics and cerebrospinal fluid pressure (CSFP) with concurrent measurement of total brain blood flow (tCBF) and regional (cervical, thoracic, and lumbar) spinal cord blood flow (SCBF). The effect of phlebotomy (to control the hemodynamic consequences of AXC) on tCBF and SCBF was assessed. Radioactive microspheres were injected at four time periods in each animal: 1) at baseline; 2) with application of the AXC; 3) after phlebotomy, to reduce the proximal mean arterial pressure (MAP(p)) to baseline values; and 4) 2 min after removal of the AXC (mean AXC time 68 +/- 6 min). With application of the AXC, the MAP(p), central venous pressure (CVP), and CSFP significantly increased (104 +/- 6 to 156 +/- 6 mmHg, 3.4 +/- 0.4 to 5.2 +/- 0.7 mmHg, and 3.3 +/- 0.7 to 5.2 +/- 0.8 mmHg, respectively), while distal mean aortic pressure (MAP(d)) significantly decreased (98 +/- 6 to 14 +/- 1 mmHg). Phlebotomy (24 +/- 3 ml.kg-1) significantly decreased MAP(p) (to 106 +/- 6 mmHg), CVP (to 1.6 +/- 0.6 mmHg), and CSFP (to 1.2 +/- 1.1 mmHg). The CSFP changed in parallel with the changes in CVP, a result suggesting that the alterations in CSFP depended on cardiac preload. The spinal cord perfusion pressure (SCPP; SCPP = MAP(d)-CSFP) was unchanged after phlebotomy, since both MAP(d) and CSFP decreased. The tCBF and cervical SCBF were unchanged when MAP(p) increased by 50% with application of the AXC; this indicated that autoregulation was intact. The thoracic and lumbar SCBF significantly decreased after AXC application (17 and 6% of baseline flows, respectively). All regional SCBFs were unchanged with phlebotomy. With removal of the AXC, all regional blood flows increased above baseline values (tCBF by 33%, P = 0.002 vs. baseline; cervical SCBF by 39%, P = 0.008; thoracic SCBF by 83%, P = 0.0001; and lumbar SCBF by 59%, P = 0.05). The increase in regional blood flows in nonischemic regions (tCBF and cervical SCBF) was correlated with an increase in arterial CO2 tension (Pa(co2)) (39.5 +/- 0.5 mmHg at baseline vs. 55.4 +/- 0.4 mmHg at release of the AXC) and unrelated to the cerebral metabolic rate for oxygen (CMR(o2)) (unchanged from baseline values). The increase in Pa(co2) presumably contributed to the increased flow in the ischemic regions (thoracic and lumbar spinal cord) as well. Phlebotomy reverses the hemodynamic consequences of thoracic AXC by treating the increase in cardiac preload that occurs with this intervention. The increase in CSFP (which occurred despite intact cerebral autoregulation) also was controlled by phlebotomy, indicating that this change also depended on the increase in right heart filling pressure.